Background

Sediments function as a secondary and significant source of tributyltin (TBT) and triphenyltin (TPT) in aquatic ecosystems and may pose a potential threat on benthic organisms and human health. The subchronic toxicity of sediment-associated TBT or TPT to snails Bellamya aeruginosa at environmentally relevant concentrations was investigated in this study. Multiple endpoints at the biochemical [ethoxyresorufin-O-deethylase (EROD), superoxide dismutase (SOD), catalase (CAT), protein carbonyl content (PCC) and lipid peroxidation (LPO)] and transcriptomic levels were examined.

Results

TBT or TPT in sediment could induce antioxidant enzymes’ activities and result in oxidative damage in the hepatopancreas of B. aeruginosa after 28-day exposure. A transcriptomic profile of B. aeruginosa exposed to TBT and TPT was reported. CYP genes and EROD activity were sensible and reliable biomarkers for toxicity assessment of TBT or TPT in sediments. Comparative pathway analysis revealed the alteration of steroid hormone biosynthesis and retinol metabolism in B. aeruginosa after 90-day exposure to sediment-associated TBT at the concentration of 2000 ng/g dw, which might affect both reproduction and lipogenesis functions. The ubiquitin proteasome system and immune system might be the toxicity target in B. aeruginosa after exposure to sediment-associated TPT for 90 days.

Conclusions

The results offered new mechanisms underlying the toxicity of sediment-associated tributyltin and triphenyltin.

中文翻译：

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蜗牛在暴露于沉积物中三丁基锡和三苯基锡的铜绿贝拉米犬中生物标志物响应和比较毒性途径的综合评估

背景

沉积物在水生生态系统中是三丁基锡（TBT）和三苯基锡（TPT）的次要和重要来源，可能对底栖生物和人类健康构成潜在威胁。在这项研究中，研究了与沉积物相关的TBT或TPT对蜗牛在环境相关浓度下对铜绿贝拉米亚虫的亚慢性毒性。检查了生化指标[乙氧基间苯二酚-O-脱乙基酶（EROD），超氧化物歧化酶（SOD），过氧化氢酶（CAT），蛋白羰基含量（PCC）和脂质过氧化（LPO）]的多个终点和转录组水平。

结果

暴露28天后，沉积物中的TBT或TPT可能诱导抗氧化酶的活性，并导致铜绿假单胞菌肝胰腺的氧化损伤。据报道，暴露于TBT和TPT的铜绿假单胞菌的转录组特征。CYP基因和EROD活性是评估沉积物中TBT或TPT毒性的明智而可靠的生物标记。比较路径分析显示，暴露于2000 ng / g dw的沉积物相关TBT 90天后，铜绿假单胞菌中类固醇激素的生物合成和视黄醇代谢发生变化，这可能会影响生殖和脂肪生成功能。泛素蛋白酶体系统和免疫系统可能是铜绿假单胞菌的毒性靶标 暴露于沉积物相关的TPT中90天后。

结论

结果提供了与沉积物相关的三丁基锡和三苯基锡毒性的新机制。